{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T23:14:26Z","timestamp":1791242066882,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2011,8,1]],"date-time":"2011-08-01T00:00:00Z","timestamp":1312156800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>A major pathological feature of chronic airway diseases is the elevated expression of gel-forming mucins. NF-\u03baB activation in airway epithelial cells has been shown to play a proinflammatory role in chronic airway diseases; however, the specific role of NF-\u03baB in mucin gene expression has not been characterized. In this study, we show that the proinflammatory cytokines, IL-1\u03b2 and IL-17A, both of which use the NF-\u03baB pathway, are potent inducers of MUC5B mRNA expression in both well differentiated primary normal human bronchial epithelial cells and the human bronchial epithelial cell line, HBE1. MUC5B induction by these cytokines was both time- and dose-dependent, and was attenuated by the small molecule inhibitor, NF-\u03baB inhibitor III, as well as p65 small interfering RNA, suggesting that the regulation of MUC5B expression by these cytokines is via an NF-\u03baB\u2013based transcriptional mechanism. Deletion analysis of the MUC5B promoter demonstrated that IL-1\u03b2\u2013 and IL-17A\u2013induced promoter activity resides within the \u22124.17-kb to \u22122.56-kb region relative to the transcriptional start site. This region contains three putative \u03baB-binding sites (NF-\u03baB-1, \u22123,786\/\u22123,774; NF-\u03baB-2, \u22123,173\/\u22123,161; and NF-\u03baB-3, \u22122,921\/\u22122,909). Chromatin immunoprecipitation analysis confirmed enhanced binding of the p50 NF-\u03baB subunit to the NF-\u03baB-3 site after cytokine stimulation. We conclude that an NF-\u03baB-based transcriptional mechanism is involved in MUC5B regulation by IL-1\u03b2 and IL-17A in airway epithelium. This is the first demonstration of the participation of NF-\u03baB and its specific binding site in cytokine-mediated airway MUC5B expression.<\/jats:p>","DOI":"10.1165\/rcmb.2009-0313oc","type":"journal-article","created":{"date-parts":[[2010,10,8]],"date-time":"2010-10-08T23:03:14Z","timestamp":1286578994000},"page":"246-252","source":"Crossref","is-referenced-by-count":131,"title":["NF-\u03baB Mediates IL-1\u03b2\u2013 and IL-17A\u2013Induced\n                    <i>MUC5B<\/i>\n                    Expression in Airway Epithelial Cells"],"prefix":"10.1093","volume":"45","author":[{"given":"Tomoyuki","family":"Fujisawa","sequence":"first","affiliation":[{"name":"Center of Comparative Respiratory Biology and Medicine, University of California at Davis, Davis, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary Mann-Jong","family":"Chang","sequence":"additional","affiliation":[{"name":"Center of Comparative Respiratory Biology and Medicine, University 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University of California at Davis, Davis, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Newton","family":"Phuong","sequence":"additional","affiliation":[{"name":"Center of Comparative Respiratory Biology and Medicine, University of California at Davis, Davis, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yin","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, Arizona"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reen","family":"Wu","sequence":"additional","affiliation":[{"name":"Center of Comparative Respiratory Biology and Medicine, University of California at Davis, Davis, California; 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